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The histone deacetylase inhibitor,trichostatin A,inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice
Authors:Tae-Ho Kim  Jung-A Jung  Gun-Dong Kim  An-Hee JangJeong-Je Cho  Yong Seek ParkCheung-Seog Park
Affiliation:Department of Microbiology (BK21), College of Medicine, Kyung Hee University, Seoul 130 701, Republic of Korea; Medical Research Center (MRC), College of Medicine, Kyung Hee University, Seoul, Republic of Korea
Abstract:
Repetitive skin contact with a chemical hapten like 2,4-dinitrofluorobenzene (DNFB) evokes an atopic dermatitis (AD)-like dermatitis reaction in NC/Nga mice maintained under specific pathogen-free (SPF) conditions. The histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), modulates the expression of several genes by inhibiting the activity of HDACs. Furthermore, TSA has been reported to suppress inflammatory cytokine expression and to induce T cell-suppression by increasing regulatory T cell (T reg cell) numbers. In addition, histone deacetylase inhibitors (HDACi) are currently undergoing clinical trials for the treatment of inflammatory disorders.
Keywords:Trichostatin A   Atopic dermatitis   2,4-dinitrofluorobenzene (DNFB)   NC/Nga   CD4+ T cells
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